Orbital Cellulitis Follow-up
- Author: John N Harrington, MD, FACS; Chief Editor: Hampton Roy Sr, MD more...
Further Inpatient Care
Closely monitor the patient (at least daily), with vision reevaluated by standardized vision testing, as appropriate, and preferably by the same examiner. Evaluate the antibiotic coverage daily and change as needed depending on the results of cultures and the patient's clinical course.[19] Repeat CT scans if the patient's condition worsens or does not respond to appropriate antibiotics.
Once the patient is clearly improving and has been afebrile for at least 48 hours, the patient can be changed from intravenous antibiotics to oral antibiotics (eg, ampicillin, cefpodoxime, cefuroxime, cefprozil) for aerobic infections or metronidazole for anaerobic infections.
Further Outpatient Care
The patient should be monitored by an infectious disease specialist, as well as an ophthalmologist, until the infectious disease specialist believes that the medications can be discontinued.
Inpatient & Outpatient Medications
See Medication.
Transfer
If necessary, the patient may be transferred for further diagnostic evaluation or for surgical intervention.
Deterrence/Prevention
No foolproof method for the prevention of orbital cellulitis exists; however, proper treatment of conditions that may precipitate orbital cellulitis (eg, preseptal cellulitis, sinusitis, dental disease) is the best deterrent.
Complications
Either orbital or intracranial complications of orbital cellulitis may occur. Subperiorbital or orbital abscess formation may occur (7-9%) or permanent vision loss may occur from corneal damage secondary to exposure or neurotrophic keratitis, destruction of intraocular tissues, secondary glaucoma, optic neuritis, or central retinal artery occlusion. Blindness also may occur secondary to elevated intraorbital pressure or direct extension of infection to the optic nerve from the sphenoid sinus. Direct involvement of the ocular motor nerves or the extraocular muscles may lead to decreased ocular motility.
Intracranial complications include meningitis (2%), cavernous sinus thrombosis (1%), and intracranial, epidural, or subdural abscess formation. Although cavernous sinus thrombosis has become relatively rare in developed countries with proper treatment, it has a mortality rate of 50% or higher. Cavernous sinus should be considered in any patient with orbital cellulitis and suspected in the presence of rapid progression of the clinical signs (eg, increasing proptosis, mydriasis, dilation of retinal veins, decreasing visual acuity, development of an afferent pupillary defect).
Intracranial abscess formation is suggested by altered consciousness, signs of central nervous system disturbance, persistent fever despite adequate antibiotic therapy, and resolution of the sinusitis and orbital cellulitis components of the disease.
Orbital cellulitis resulting from sinusitis usually can be distinguished easily from other causes of acute inflammatory proptosis by clinical signs, CT scans, and assessment of risk factors.
Cavernous sinus thrombosis, a serious complication of paranasal sinusitis that most commonly results from anterograde spread from infection involving the mid third of the face (eg, orbit, mouth, paranasal sinuses), may be difficult to distinguish from simple orbital cellulitis. It may occur with and be caused by orbital cellulitis. A patient with cavernous sinus thrombosis without orbital cellulitis will show marked restriction of ocular motility out of proportion to the degree of proptosis. A patient also will have normal retropulsion of the globe, hypesthesia in the distribution of the first and second divisions of the trigeminal nerve, dilated retinal veins, orbital congestion, and possibly neurologic defects (eg, altered sensorium). A cranial MRI can help confirm the diagnosis of cavernous sinus thrombosis.
Orbital pseudotumor may cause rapidly developing orbital congestion, proptosis, and limitation of motility, but it typically occurs in older age groups. Orbital echography may be helpful in differentiation.
Usually, endocrine orbitopathy may be identified by its typical clinical features. Orbital myositis may produce mild vascular congestion and proptosis. A fast-growing necrotic retinoblastoma may produce mild vascular congestion, proptosis, and rhabdomyosarcoma. Metastatic orbital tumor, especially breast carcinoma, may give similar findings.
Patient Education
For excellent patient education resources, see eMedicine's Diabetes Center. Also, visit eMedicine's patient education article Cellulitis.
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